The proportion of the child and adolescent population that is in appropriate energy balance is declining throughout the developed world, and childhood obesity is a particular problem in the UK relative to other northern European countries. Assessment of the underlying causes of obesity, and the different routes to its development, may assist in the definition of successful intervention strategies. The network of peripheral and central (brain) regulatory systems that underlie energy balance and body weight and composition can, for the most part, only be approached experimentally through the study of appropriate laboratory animal models. This problem is particularly acute when the target is overweight and obesity in the young. Some of the mechanisms underlying the development of energy imbalance and specifically the onset of overweight and obesity in the young, and the metabolic health consequences of obesity, can be addressed by examination of experimental rodent models in which mutation of a single gene causes early-onset extreme obesity, genetic susceptibility to obesity is revealed in an obesogenic environment or early-life nutritional experience programmes susceptibility to obesity or metabolic problems in later life. These studies highlight genes that are essential to normal body-weight regulation in rodents and man, the impact of diet and diet-induced obesity on regulatory systems in the young and the potential sensitivity of developing regulatory systems to nutritional experiences in utero and during early life.

During the past decades there has been considerable interest in the use of dietary fibre in both animal and human nutrition. In human subjects dietary fibre has been studied intensively for possible effects on body-weight management and health. In animal nutrition the interest in dietary fibre has increased because it can be used as a cheap source of energy and because of its potential to improve animal welfare and reduce abnormal (mainly stereotypic) behaviour. Animal welfare is impaired if the diet does not provide sufficient satiety, combined with an environment that does not meet specific behavioural requirements related to natural feeding habits (e.g. rooting in pigs). A considerable proportion of the behavioural effects of dietary fibre are thought to be related to reduced feeding motivation. It has been hypothesized that: (1) bulky fibres increase satiety and thereby decrease physical activity and stereotypic behaviours immediately following a meal in pigs; (2) fermentable fibres prolong postprandial satiety and thereby reduce physical activity and appetitive behaviours for many hours after a meal. The validity of these hypotheses is examined by considering published data. In sows dietary fibres (irrespective of source) reduce stereotypic self-directed behaviours and substrate-directed behaviours, and to a lesser extent overall physical activity, indicating enhanced satiety shortly after a meal. Furthermore, fermentable dietary fibre reduces substrate-directed behaviour in sows and physical activity in sows and growing pigs for many hours after a meal. Evidence of long-term effects of poorly-fermentable fibre sources is inconclusive. The findings suggest that highly-fermentable dietary fibres have a higher potential to prolong postprandial satiety.

Childhood obesity has multiple causes, most of them capable of explaining only one part of the problem. The population-wide impact of sedentary lifestyles and availability of energy-dense food is undeniable, but substantial individual differences in body weight persist, suggesting that individuals respond differently to the ‘obesogenic’ environment. One plausible mechanism for this variation is the early expression of appetitive traits, including low responsiveness to internal satiety signals, high responsiveness to external food cues, high subjective reward experienced when eating liked foods and preferences for energy-dense foods. Case–control studies support the existence of abnormalities in these traits among obese children compared with normal-weight children, and correlations between psychometric measures of child appetite and child weight suggest that appetitive trait profiles may not only promote obesity but also protect against it. The origins of appetitive traits are as yet uncharted, but will include both genetic and environmental influences. Parental feeding style may affect the development of appetite but the exact nature of the relevant behaviours is unclear and many studies are cross-sectional or begin late in childhood, obscuring causal relationships. Future research should explore determinants and biological mechanisms by using prospective designs beginning early in life, measuring relevant biomarkers such as gut hormones and incorporating neuroimaging and genotyping technologies. Potential clinical applications include the identification of ‘at risk’ children early in life and interventions to modify appetitive traits or ameliorate their impact on intake and weight.

Obesity in children is difficult to treat, but it seems to be easier to treat than adult obesity. The first step in treatment is to identify effective advice relating to nutrition and physical activity. In most treatment studies the macronutrient composition of the diet is not of major importance for treatment outcome. In relation to physical activity fat-utilisation strategies have been described. The second step includes appropriate approaches to lifestyle change. In Europe there are no drugs approved for children, and surgery for children is still limited to research projects. Thus, the major challenge is to develop effective ways of changing lifestyle. Family therapy may be an effective approach in preventing severe obesity from developing during puberty, and a therapeutic strategy based on treatment studies is described. The family-therapy techniques used here are intended to facilitate the family's own attempts to modify their lifestyle, and to increase their own sense of responsibility and readiness to change, i.e. these variables are the prime targets during therapy. Thus, the family, not the therapist, assumes responsibility for the changes achieved. This approach may be helpful in making the therapeutic process less cumbersome for the therapist. Instead of the therapist attempting to persuade the obese subjects to lose weight, it might be more effective to teach them to control their eating patterns through their own efforts. The treatment model includes structural family therapy and solution-focused-brief therapy. The use of such a model makes it possible to train therapists and health professionals to use an evidence-based intervention model.

There is now considerable evidence from several data sources, including the National Surveys of Lifestyles, Attitudes and Nutrition, that dietary patterns vary according to social position in the Republic of Ireland and those individuals in situations of social disadvantage experience barriers to consuming a healthy diet according to recommended guidelines. Obesity is a major impending public health problem related in part to social position that requires concerted inter-sectoral policy action. The Life-ways Cross-generation Cohort Study of >1000 Irish families has been followed prospectively since antenatal recruitment in 2001. Published findings to date indicate considerable social variability in food consumption and BMI patterns during pregnancy in the case of the maternal cohort. The present paper reports nutrient intake across the four family cohorts related to a key variable of interest, means-tested General Medical Services eligibility.

Breast-feeding is the superior infant feeding method from birth, with research consistently demonstrating its numerous short- and long-term health benefits for both mother and infant. As a global recommendation the WHO advises that mothers should exclusively breast-feed for the first 6-months of life, thus delaying the introduction of solids during this time. Historically, Irish breast-feeding initiation rates have remained strikingly low in comparison with international data and there has been little improvement in breast-feeding duration rates. There is wide geographical variation in terms of breast-feeding initiation both internationally and in Ireland. Some of these differences in breast-feeding rates may be associated with differing socio-economic characteristics. A recent cross-sectional prospective study of 561 pregnant women attending a Dublin hospital and followed from the antenatal period to 6 months post partum has found that 47% of the Irish-national mothers initiated breast-feeding, while only 24% were still offering ‘any’ breast milk to their infants at 6 weeks. Mothers' positive antenatal feeding intention to breast-feed is indicated as one of the most important independent determinants of initiation and ‘any’ breast-feeding at 6 weeks, suggesting that the antenatal period should be targeted as an effective time to influence and affect mothers' attitudes and beliefs pertaining to breast-feeding. These results suggest that the ‘cultural’ barrier towards breast-feeding appears to still prevail in Ireland and consequently an environment that enables women to breast-feed is far from being achieved. Undoubtedly, a shift towards a more positive and accepting breast-feeding culture is required if national breast-feeding rates are to improve.

Adequate intake of folic acid by women during very early pregnancy can markedly reduce risk of the development of neural-tube defects (NTD). The effectiveness of advice to women to take folic acid supplements is limited, mainly because 50% of pregnancies are unplanned. However, mandatory folic acid food fortification programmes in North America have been very successful in reducing NTD rates. In Ireland higher rates of pregnancies are affected by NTD and the option of termination is illegal. Consequently, the much higher burden of disease makes primary prevention of NTD an important public health issue in Ireland. During 2006 a decision was taken in Ireland to initiate mandatory folic acid fortification of most bread to prevent NTD. Priority work was immediately undertaken to establish reliable and comprehensive baseline information on factors that will be affected by fortification. This information included data on: the national prevalence of pregnancies affected by NTD; the current extent of voluntary folic acid fortification of food on the Irish market and how it affects folic acid intakes; blood folate status indicators assessed for various subgroups of the Irish population. In addition, scientific developments that have arisen since 2006 relating to the risks and benefits of folic acid intake are under ongoing review. The present paper summarises the rationale for mandatory folic acid food fortification in Ireland and recent scientific developments relating to risks and benefits of folic acid intake. In this context, preliminary findings of baseline monitoring investigations in Ireland are considered.

Epigenetics encompasses changes to marks on the genome that are copied from one cell generation to the next, which may alter gene expression but which do not involve changes in the primary DNA sequence. These marks include DNA methylation (methylation of cytosines within CpG dinucleotides) and post-translational modifications (acetylation, methylation, phosphorylation and ubiquitination) of the histone tails protruding from nucleosome cores. The sum of genome-wide epigenetic patterns is known as the epigenome. It is hypothesised that altered epigenetic marking is a means through which evidence of environmental exposures (including nutritional status and dietary exposure) is received and recorded by the genome. At least some of these epigenetic marks are remembered through multiple cell generations and their effects may be revealed in altered gene expression and cell function. Altered epigenetic marking allows plasticity of phenotype in a fixed genotype. Despite their identical genotypes, monozygotic twins show increasing epigenetic diversity with age and with divergent lifestyles. Differences in epigenetic markings may explain some inter-individual variation in disease risk and in response to nutritional interventions.

The Human Genome Project and rapid advances in high-throughput molecular technologies are providing an unprecedented opportunity to advance the understanding of the common polygenic diet-related diseases, including obesity, the metabolic syndrome, type 2 diabetes mellitus, CVD and some cancers. In particular, transcriptomic approaches that allow multiple simultaneous gene-expression profiles facilitate the characterisation of metabolic perturbations that underlie diet-related pathologies. The present paper will focus on ‘transcriptomic signatures’ to characterise and understand the molecular mechanisms that accurately reflect ‘metabolic health’.

Metabolomics aims to profile all small molecules that are present in biological samples such as biofluids, tissue extracts and culture media. Combining the data obtained with multivariate data analysis tools allows the exploration of changes induced by a biological treatment or changes resulting from phenotype. Recently, there has been a large increase in interest in using metabolomics in nutritional research and because of the intimate relationship between nutrients and metabolism there exists great potential for the use of metabolomics within nutritional research. However, for metabolomics to reach its full potential within this field it is also important to be realistic about the challenges that are faced. Examples of such challenges include the necessity to have a clear understanding of the causes of variation in human metabolomic profiles, the effects of the gut microflora on the metabolomic profile and the interaction of the gut microflora with the host's metabolism. A further challenge that is particularly relevant for human nutritional research is the difficulty associated with biological interpretation of the data. Notwithstanding these and other challenges, several examples of successful applications to nutritional research exist. The link between the human metabolic phenotype, as characterised by metabolomic profiles, and dietary preferences proposes the potential role of metabolomics in personalised nutrition.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease manifested by swollen and painful joints, bone erosion and functional impairment. The joint lesions are characterised by infiltration of T lymphocytes, macrophages and B lymphocytes into the synovium and by synovial inflammation involving eicosanoids, cytokines and matrix metalloproteinases. In relation to inflammatory processes, the main fatty acids of interest are the n-6 PUFA arachidonic acid, which is the precursor of inflammatory eicosanoids such as PGE2 and leukotriene B4, and the n-3 PUFA EPA and DHA, which are found in oily fish and fish oils. Eicosanoids derived from the n-6 PUFA arachidonic acid play a role in RA, and the efficacy of non-steroidal anti-inflammatory drugs in RA indicates the importance of pro-inflammatory cyclooxygenase pathway products of arachidonic acid in the pathophysiology of the disease. EPA and DHA inhibit arachidonic acid metabolism to inflammatory eicosanoids. EPA also gives rise to eicosanoid mediators that are less inflammatory than those produced from arachidonic acid and both EPA and DHA give rise to resolvins that are anti-inflammatory and inflammation resolving. In addition to modifying the lipid mediator profile, n-3 PUFA exert effects on other aspects of immunity relevant to RA such as antigen presentation, T-cell reactivity and inflammatory cytokine production. Fish oil has been shown to slow the development of arthritis in an animal model and to reduce disease severity. Randomised clinical trials have demonstrated a range of clinical benefits in patients with RA that include reducing pain, duration of morning stiffness and use of non-steroidal anti-inflammatory drugs.

Despite the acknowledged benefits of reducing SFA intake few countries within the EU meet recognised targets. Milk and dairy products represent the single largest source of dietary SFA in most countries, yet epidemiological evidence indicates that milk has cardioprotective properties such that simply reducing consumption of dairy foods to meet SFA targets may not be a sound public health approach. The present paper explores the options for replacing some of the SFA in milk fat with cis-MUFA through alteration of the diet of the dairy cow, and the evidence that such changes can improve the indicators for CHD and CVD in general for the consumer. In addition, the outcome of such changes on risk factors for CHD and CVD at the population level is examined in the light of a modelling exercise involving data for eleven EU member states. Given the current and projected costs of health care, the results indicate that urgent consideration should be given to such a strategy.

One of the key challenges facing efforts to translate nutrition research into public health recommendations is understanding how the public will respond to these efforts, including whether they will trust the information. Among factors that influence trust in health communication is the extent to which the sources of the information are considered accurate, balanced, fair and unbiased. In relation to bias, few issues rise to as high a level of concern as the suspicion of conflicts of interest among scientists. Sometimes, even the perception of conflict of interest is enough to cast doubt on the integrity of the research and credibility of the results. The present paper provides an overview of research on conflicts of interest in science, including ways in which it has touched the field of nutrition. It then offers data on public views about conflicts of interest in science, including the extent to which funding sources influence trustworthiness of the research. The conclusions suggest implications for translational research in nutrition.

Accurate assessment of maternal micronutrient status is critical to the prevention of suboptimal micronutrient status and anaemia during pregnancy. Measurement of Fe, folate and vitamin B12 status is complicated by adaptive changes to maternal and placental physiology that markedly affect concentrations of circulating micronutrients and their functional biomarkers. Validation of new assessment methods by comparison with gold standards is often prevented by ethical considerations. Antenatal screening in the UK is predominantly concerned with the detection of anaemia, although estimation of maternal Fe stores by serum ferritin at the start of antenatal care may be a more effective preventive strategy. Functional assessment of maternal anaemia is highly problematic, so instead reference data are used for its definition. The effect of mild-to-moderate anaemia on pregnancy outcome is unclear because of the crude nature of its assessment and the influence of confounding factors. Fe-deficient erythropoiesis may be detected by assessment of erythrocyte Zn protoporphyrin and reticulocyte Hb, although such measures may be unavailable in many clinical laboratories. Serum soluble transferrin receptor is highly responsive to tissue Fe deficiency and is less affected by inflammation than most other indicators. Direct inter-assay comparison of serum and erythrocyte folate values is inadvisable since recovery rates differ greatly between methods. Serum total homocysteine is a useful functional biomarker of both folate and vitamin B12 status but during pregnancy is influenced by other factors that reduce its sensitivity. Isotope-dilution liquid chromatography–tandem MS and serum holo-transcobalamin provide new opportunities to gain detailed data of folate species and vitamin B12 fractions in large samples.